Pituitary neuroendocrine tumours, also known as pituitary adenomas1, are benign neoplasms reported to occur in up to 20% of the population2. Thyroid stimulating hormone (TSH) secreting tumours are rare and account for 0.5-3% of all pituitary neuroendocrine tumours3; with only 20% of these co-secreting growth hormone (GH) or prolactin (PRL) due to their shared Pituitary transcription factor 1 (Pit-1) lineage3,4,5. Plurihormonal Pit-1 tumours are also known for their aggressive nature4.
We report a case of a 34 year old male presenting in 2019 with clinical symptoms of lethargy, insomnia, tremor, palpitations and tachycardia. Biochemistry showed evidence of hyperthyroidism (fT4 29.1pmol/L, fT3 12.6pmol/L) with inappropriately normal TSH (TSH 3.5mU/L,) and elevated IGF-1 77nmol/L (RR14-40nmol/L). Magnetic resonance imaging (MRI) demonstrated a 30 x 27 x 24m pituitary macroadenoma and he subsequently underwent transsphenoidal resection, with histopathology consistent with a plurihormonal PIT-1 positive, TSH and GH-secreting tumour. Post-operative imaging showed evidence of a small 4mm residual tumour and he developed post-operative panhypopituitarism with likely growth hormone deficiency but ongoing TSH hypersecretion.
Though rare, there are previous case reports of co-secreting TSH and GH pituitary neuroendocrine tumours3,6,7,8,9, cured through surgical intervention alone3,7, requiring adjuvant use of somatostatin analogs6,9, concomitant use of a somatostatin analog and Pegvisomant8 and also a case of resistance to somatostatin analogue after surgery10. Adjuvant radiotherapy is an option but has a low remission rate of 60%8.
In our patient, medical management poses a dilemma; Lanreotide 60mg every 6 months controls TSH secretion and residual tumour size remains stable, but leads to further reduction of GH levels and significantly contributes to fatigue and reduced quality of life. To date he continues to await surgical resection of his residual tumour.